Evidence map›Paper›PMID 30073506›Full record

ArticleMolecular neurobiology2019

Treadmill Exercise Attenuates L-DOPA-Induced Dyskinesia and Increases Striatal Levels of Glial Cell-Derived Neurotrophic Factor (GDNF) in Hemiparkinsonian Mice.

Ana E Speck, Marissa G Schamne, Aderbal S Aguiar, Rodrigo A Cunha, Rui D Prediger

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In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
1.6field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Ana E SpeckGraduate Program of Neuroscience, Center of Biological Sciences, Federal University of Santa Catarina (UFSC), Florianópolis, Brazil.
Marissa G SchamneDepartment of Pharmacology, Center of Biological Sciences, Federal University of Santa Catarina (UFSC), Florianópolis, 88049-900, Brazil.
Aderbal S AguiarGraduate Program of Neuroscience, Center of Biological Sciences, Federal University of Santa Catarina (UFSC), Florianópolis, Brazil.
Rodrigo A CunhaCNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal.
Rui D PredigerGraduate Program of Neuroscience, Center of Biological Sciences, Federal University of Santa Catarina (UFSC), Florianópolis, Brazil. ruidsp@hotmail.com.ORCID http://orcid.org/0000-0002-7547-6463
Universidade Federal de Santa Catarina · BRUniversity of Coimbra · PT

Funding

Universal CNPq 408676/2016-7
6 · The paper itself

Abstract

Exercise can act as a disease-modifying agent in Parkinson's disease (PD), and we have previously demonstrated that voluntary exercise in running wheels during 2 weeks normalizes striatopallidal dopaminergic signaling and prevents the development of L-DOPA-induced dyskinesia (LID) in C57BL/6 mice. We now tested whether LID in Swiss albino mice could be attenuated by treadmill-controlled exercise alone or in combination with the reference antidyskinetic drug amantadine. The daily intraperitoneal (i.p.) treatment with three different doses of L-DOPA/benserazide (30/12.5, 50/25, or 70/35 mg/kg) during 3 weeks induced increasing levels of LID scores in hemiparkinsonian Swiss albino mice previously lesioned with a unilateral intrastriatal injection of 6-hydroxydopamine (6-OHDA, 10 μg). Then, we addressed the antidyskinetic effects of treadmill-controlled exercise by comparing LID, induced by L-DOPA/benserazide (50/25 mg/kg, i.p.) during 4 weeks, in sedentary and daily exercised mice. Exercise reduced LID and improved motor skills of dyskinetic mice, as indicated by decreased contralateral bias, increase in maximal load test, and latency to fall in rotarod. The antidyskinetic effect of amantadine (60 mg/kg, i.p.) was only observed in sedentary mice, indicating the absence of synergistic antidyskinetic effect of the combination of treadmill exercise plus amantadine. Finally, Western blot analysis unraveled an ability of exercise to increase the striatal immunocontent of glial cell-derived neurotrophic factor (GDNF), apart from normalizing striatal levels of tyrosine hydroxylase. These findings show that controlled treadmill exercise attenuates LID and provide the first indication that the antidyskinetic effects of treadmill exercise may involve increased striatal GDNF levels.

Indexed as

Physical Conditioning, AnimalAnimalsCorpus StriatumDisease Models, AnimalDopamine Plasma Membrane Transport ProteinsDyskinesia, Drug-InducedGlial Cell Line-Derived Neurotrophic FactorLevodopaMaleMice, Inbred C57BLMotor ActivityParkinson DiseaseTyrosine 3-MonooxygenaseDopamine Plasma Membrane Transport ProteinsGlial Cell Line-Derived Neurotrophic FactorLevodopaTyrosine 3-Monooxygenase6-OHDADyskinesiaExerciseGDNFL-DOPAParkinson’s diseaseTreadmill

Identifiers

PMID30073506
OpenAlexW2886619398

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.